GTF2H2通过介导AKT信号通路影响肝癌细胞Hep3B的增殖和迁移

GTF2H2 Affects the Proliferation and Migration of Hep3B Hepatocellular Carcinoma Cells by Mediating AKT Signal Pathway

目的:探讨通用转录因子II H亚基2(GTF2H2)是否影响肝癌细胞Hep3B的增殖和迁移及其潜在的分子机制。方法:通过转染GTF2H2-siRNA构建GTF2H2敲低的Hep3B肝癌细胞模型;实时定量聚合酶链反应(q-RT-PCR)和蛋白质印迹实验检测肝癌细胞Hep3B的GTF2H2敲低效果;细胞计数实验(MTS)检测GTF2H2敲低的肝癌细胞Hep3B的增殖能力;Transwell细胞迁移实验检测GTF2H2敲低的肝癌细胞Hep3B的迁移能力;蛋白质印迹分析实验检测GTF2H2敲低后是否影响肿瘤相关分子信号通路。结果:GTF2H2敲低组的Hep3B细胞的增殖能力较对照组的Hep3B细胞增强,迁移能力亦有增强;蛋白质印迹实验显示GTF2H2敲低后,p-AKT通路蛋白的表达明显升高。结论:GTF2H2可能通过介导AKT分子信号通路,影响肝癌细胞Hep3B的增殖和迁移能力。

Objective:To investigate whether General transcription factorⅡsubunit 2(GTF2H2)affects the proliferation and migration of Hep3B cells and the underlying molecular mechanism.Methods:The GTF2H2 knockdown Hep3B cell model was constructed by transfecting GTF2H2-siRNA.Quantitative real-time polymerase chain reaction and Western blotting were used to detect the GTF2H2 knockdown effect in Hep3B cells.MTS cell proliferation assay kit was used to detect the proliferation ability of GTF2H2 knockdown Hep3B cells.The migration ability of GTF2H2 knockdown Hep3B cells was evaluated by cell Transwell assay.Western blotting was used to detect whether GTF2H2 knockdown affects tumor associated molecular signaling pathway.Results:The proliferation and migration ability of GTF2H2 knockdown Hep3B cells was stronger than that of the controls.Western blotting showed that the expression of p-AKT pathway protein in GTF2H2 knockdown Hep3B cells was significantly increased.Conclusion:GTF2H2 may affect the proliferation and migration ability of Hep3B cells by the regulation of the AKT molecular signal pathway.